Second edition

10.qxd 3/10/08 5:52 PM Page 434
434 Vascular disorders
Etiology
In most cases, the dementia occurs secondary to bilateral,
multiple, territorial large vessel infarctions involving the
frontal, parietal, and temporal cortices (Erkinjunti et al. 1988;
Jayakumar et al. 1989; Ladurna et al. 1982; Liu et al. 1992;
Tomlinson et al. 1970); rarely, single infarctions, for example
in the temporal or frontal lobes, may be responsible (Auchus
et al. 2002; Yoshitake et al. 1995). Although most cases are
due to infarction, as the name ‘multi-infarct’ suggests, a very
similar clinical picture can emerge with multiple intracerebral
hemorrhages, and it is probably appropriate to lump these
cases under the rubric of multi-infarct dementia. A better
name might be ‘multi-stroke’ dementia, but the term multiinfarct
has great currency and probably will not change.
The multiple causes of these infarctions (and hemorrhages)
are discussed in Section 7.4.
Differential diagnosis
The diagnosis of multi-infarct dementia should be considered
in any patient with dementia and a history of stroke.
In weighing this history, however, one must take into
account the location of the lesion: whereas infarcts in such
cognitively strategic locations as the frontal, parietal, or
temporal cortices might be expected to cause dementia,
one would be hard-pressed to attribute a dementia to
infarctions occurring in the occipital lobes.
Lacunar dementia may also present with a history of
stroke; however, here the strokes tend to be of the lacunar
variety, such as pure motor stroke. Furthermore, and in
contrast to multi-infarct dementia, lacunar dementia tends
to be characterized by a frontal lobe syndrome.
As noted earlier, it is not uncommon to find patients
with more than one vascular process underlying a dementia,
and in such cases MR scanning is generally necessary to
determine the various contributions of cortical infarctions,
lacunar infarctions, and diffuse white matter disease. In
some instances, it may not be possible to disentangle the
effects of each of these separate processes, and in such
cases, one may have to be content with merely making a
diagnosis of vascular dementia.
Given the prevalence of Alzheimer’s disease, it must
also be borne in mind that it is not at all uncommon to find
patients with a ‘mixed’ dementia, that is with a combination
of multi-infarct dementia and Alzheimer’s disease
(Tomlinson et al. 1970). Such a diagnosis should be considered
in cases in which the course is mixed, being composed
of sequential downward steps occurring on a
background of a steady, gradual decline.
Treatment
The general treatment of dementia is discussed in Section
5.1. Antidepressants, for example a selective serotonin
reuptake inhibitor (SSRI), may be needed for depressive
symptoms, and antipsychotics, such as risperidone, for hallucinations,
delusions, and agitation. There is also evidence
that both the cholinesterase inhibitors donepezil (Black et al.
2003; Wilkinson et al. 2003) and galantamine (Auchus et al.
2007), and memantine (Orgogozo et al. 2002; Wilcock
et al. 2002) may improve overall cognitive function.
Concurrent with symptomatic treatment, steps should
be taken to prevent future strokes if possible, as discussed
in Section 7.4.
10.2 LACUNAR DEMENTIA
As discussed in Section 7.4, lacunes are small cavities that
may be found in the thalamus, basal ganglia, and internal and
external capsules, among other locations, and which occur as
sequelae to infarctions in the areas of distribution of central
or perforating arteries. Single lacunes may be clinically ‘silent’
or present with one of the classic lacunar syndromes, such as
pure motor stroke. When multiple lacunes are present, one
speaks of the ‘lacunar state’; when significant cognitive
impairment occurs on the basis of multiple lacunes (or, albeit
uncommonly, on the basis of a single ‘strategically’ located
lacune) it is customary to speak of subcortical vascular
dementia or, more simply, lacunar dementia. Lacunar dementia,
along with multi-infarct dementia and Binswanger’s disease,
is a vascular dementia, and although it may occur in a
‘pure’ state, it is not uncommonly accompanied by other evidence
of vascular pathology, such as the large territorial
infarcts seen in multi-infarct dementia or the ischemic
leukoencephalopathy of Binswanger’s disease.
Although the prevalence of lacunar dementia is not
known with any precision, the clinical impression is that it
is not uncommon.
Clinical features
In addition to cognitive deficits such as decreased shortterm
memory, slowed thinking, and disorientation (Mok
et al. 2004), etc., one also classically sees elements of the
frontal lobe syndrome such as disinhibition, affective
change, perseveration or apathy (Ishii et al. 1986; Wolfe et al.
1990). In some cases, parkinsonism may occur, as discussed
in Section 10.3. As might be expected, there is typically also
a history of lacunar syndromes, such as pure motor stroke,
ataxic hemiparesis, dysarthria–clumsy hand or pure sensory
stroke. Furthermore, and in advanced cases of the lacunar
state, it is common to see a psuedobulbar palsy with, as
described in Section 4.7, emotional incontinence.
Although CT scanning may reveal some lacunes, MRI is
far more sensitive and is strongly recommended.
Course
In most cases, lacunar dementia is a progressive condition,
and the progression itself may be either ‘stepwise’ or more